Bottom Line:
A final hyperglycemic clamp was then performed.After supplementation, serum 25(OH)D was 142.7 ± 25.7 and 42.9 ± 17.3 nmol/L in 49 of 51 completing participants randomized to vitamin D and 45 of 53 randomized to placebo, respectively.At the end of the study, there were no statistically significant differences in the outcome variables between the two groups.

Objective: Vitamin D deficiency is associated with an unfavorable metabolic profile in observational studies. The intention was to compare insulin sensitivity (the primary end point) and secretion and lipids in subjects with low and high serum 25(OH)D (25-hydroxyvitamin D) levels and to assess the effect of vitamin D supplementation on the same outcomes among the participants with low serum 25(OH)D levels.

Research design and methods: Participants were recruited from a population-based study (the Tromsø Study) based on their serum 25(OH)D measurements. A 3-h hyperglycemic clamp was performed, and the participants with low serum 25(OH)D levels were thereafter randomized to receive capsules of 20,000 IU vitamin D(3) or identical-looking placebo twice weekly for 6 months. A final hyperglycemic clamp was then performed.

Results: The 52 participants with high serum 25(OH)D levels (85.6 ± 13.5 nmol/L [mean ± SD]) had significantly higher insulin sensitivity index (ISI) and lower HbA(1c) and triglycerides (TGs) than the 108 participants with low serum 25(OH)D (40.3 ± 12.8 nmol/L), but the differences in ISI and TGs were not significant after adjustments. After supplementation, serum 25(OH)D was 142.7 ± 25.7 and 42.9 ± 17.3 nmol/L in 49 of 51 completing participants randomized to vitamin D and 45 of 53 randomized to placebo, respectively. At the end of the study, there were no statistically significant differences in the outcome variables between the two groups.

Mentions:
Serum 25(OH)D increased to a mean of 142.7 nmol/L in the treatment group and remained low in the placebo group (42.9 nmol/L) with no overlap between the groups (Table 3). Conversely, plasma PTH decreased in the treatment group while remaining unchanged in the placebo group. There were no statistically significant differences between the two groups after 6 months regarding measures of insulin secretion, insulin sensitivity, or lipids (Table 3 and Figs. 3 and 4). The results were essentially the same if statin users were excluded, if the analyses were performed as intention-to-treat analyses or per-protocol analyses, or if adjustments for baseline BMI, sex, and age were performed. The treatment group had a statistically significant increase in fasting glucose and HbA1c during the study and also a slight decrease in BMI; however, these changes were not significantly different from the placebo group (Table 3). There were no statistical interactions between treatment group and sex, below/above median HOMA-IR, BMI, or dairy servings per week on the effect on ISI (P = 0.94, 0.19, 0.38, and 0.09, respectively). Accordingly, analyses stratified by sex, above/below baseline median of HOMA-IR (1.83), BMI (26.8 kg/m2), or dairy servings per week (18 servings) revealed similar results (data not shown).

Mentions:
Serum 25(OH)D increased to a mean of 142.7 nmol/L in the treatment group and remained low in the placebo group (42.9 nmol/L) with no overlap between the groups (Table 3). Conversely, plasma PTH decreased in the treatment group while remaining unchanged in the placebo group. There were no statistically significant differences between the two groups after 6 months regarding measures of insulin secretion, insulin sensitivity, or lipids (Table 3 and Figs. 3 and 4). The results were essentially the same if statin users were excluded, if the analyses were performed as intention-to-treat analyses or per-protocol analyses, or if adjustments for baseline BMI, sex, and age were performed. The treatment group had a statistically significant increase in fasting glucose and HbA1c during the study and also a slight decrease in BMI; however, these changes were not significantly different from the placebo group (Table 3). There were no statistical interactions between treatment group and sex, below/above median HOMA-IR, BMI, or dairy servings per week on the effect on ISI (P = 0.94, 0.19, 0.38, and 0.09, respectively). Accordingly, analyses stratified by sex, above/below baseline median of HOMA-IR (1.83), BMI (26.8 kg/m2), or dairy servings per week (18 servings) revealed similar results (data not shown).

Bottom Line:
A final hyperglycemic clamp was then performed.After supplementation, serum 25(OH)D was 142.7 ± 25.7 and 42.9 ± 17.3 nmol/L in 49 of 51 completing participants randomized to vitamin D and 45 of 53 randomized to placebo, respectively.At the end of the study, there were no statistically significant differences in the outcome variables between the two groups.

Objective: Vitamin D deficiency is associated with an unfavorable metabolic profile in observational studies. The intention was to compare insulin sensitivity (the primary end point) and secretion and lipids in subjects with low and high serum 25(OH)D (25-hydroxyvitamin D) levels and to assess the effect of vitamin D supplementation on the same outcomes among the participants with low serum 25(OH)D levels.

Research design and methods: Participants were recruited from a population-based study (the Tromsø Study) based on their serum 25(OH)D measurements. A 3-h hyperglycemic clamp was performed, and the participants with low serum 25(OH)D levels were thereafter randomized to receive capsules of 20,000 IU vitamin D(3) or identical-looking placebo twice weekly for 6 months. A final hyperglycemic clamp was then performed.

Results: The 52 participants with high serum 25(OH)D levels (85.6 ± 13.5 nmol/L [mean ± SD]) had significantly higher insulin sensitivity index (ISI) and lower HbA(1c) and triglycerides (TGs) than the 108 participants with low serum 25(OH)D (40.3 ± 12.8 nmol/L), but the differences in ISI and TGs were not significant after adjustments. After supplementation, serum 25(OH)D was 142.7 ± 25.7 and 42.9 ± 17.3 nmol/L in 49 of 51 completing participants randomized to vitamin D and 45 of 53 randomized to placebo, respectively. At the end of the study, there were no statistically significant differences in the outcome variables between the two groups.